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Transient increase in sAPPα secretion in response to Aβ1–42 oligomers: an attempt of neuronal self-defense?

Rose, Christiane, Dorard, Emilie, Audrain, Mickael, Gorisse-Hussonnois, Lucie, Cartier, Nathalie, Braudeau, Jérome, Allinquant, Bernadette·2018·Neurobiology of Aging
DOI 10.1016/j.neurobiolaging.2017.09.008
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Abstract

Amyloid precursor protein (APP), a key molecule of Alzheimer disease, is metabolized in 2 antagonist pathways generating the soluble APP alpha (sAPPα) having neuroprotective properties and the beta amyloid (Aβ) peptide at the origin of neurotoxic oligomers, particularly Aβ1-42. Whether extracellular Aβ1-42 oligomers modulate the formation and secretion of sAPPα is not known. We report here that the addition of Aβ1-42 oligomers to primary cortical neurons induced a transient increase in α-secretase activity and secreted sAPPα 6-9 hours later. Preventing the generation of sAPPα by using small interfering RNAs (siRNAs) for the α-secretases ADAM10 and ADAM17 or for APP led to increased Aβ1-42 oligomer-induced cell death after 24 hours. Neuronal injuries due to oxidative stress or growth factor deprivation also generated sAPPα 7 hours later. Finally, acute injection of Aβ1-42 oligomers into wild-type mouse hippocampi induced transient secretion of sAPPα 48-72 hours later. Altogether, these data suggest that neurons respond to stress by generating sAPPα for their survival. These data must be taken into account when interpreting sAPPα levels as a biomarker in neurological disorders.

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Metadata

Authors
Rose, C., Dorard, E., Audrain, M., Gorisse-Hussonnois, L., Cartier, N., Braudeau, J., & Allinquant, B.
ORCID
Braudeau, Jérome
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2018-01
Volume
61
Pages
23-35
ISSN
0197-4580
DOI
10.1016/j.neurobiolaging.2017.09.008
Cited by
12
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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